• Chao Zhang, Bingdi Xie, Xiaowen Li, and Yuanrong Yao.
• Department of Neurology, Neurological Institute, Tianjin Medical University General Hospital, Anshan Avenue 154, Heping District, Tianjin, 300052, China.
• Neurol. Sci. 2014 Aug 1; 35 (8): 1209-14.

AbstractFew objective methods have been utilized to identify the small myelinated fiber impairment causing neuropathic pain in Guillain-Barré syndrome (GBS). In this study, contact heat-evoked potentials (CHEPs) were applied to study the nociceptive pathway in GBS. Sixty GBS patients and fifty healthy controls were enrolled. The 60 GBS patients were divided into two subgroups presenting with or without subjective lower limb paresthesia (21/39). CHEPs were recorded at Cz and Pz with a peak thermal stimuli of 47 °C applied to the skin of the leg above the internal malleolus (AIM) and of the waist at the anterior superior iliac spine (ASIS) level. The N2 latency and N2-P2 amplitude of CHEPs were compared. When the skin of the leg AIM was stimulated, the N2 latency was significantly postponed (425.23 ± 28.66 vs. 402.30 ± 19.48 ms, P < 0.05) and the N2-P2 amplitude significantly decreased in GBS patients as compared to controls (32.71 ± 7.49 vs. 42.77 ± 8.71 μV, P < 0.05). Slower nerve conduction velocity was observed in GBS patients (11.84 ± 1.45 vs. 13.28 ± 0.66 ms, P < 0.05). However, no differences in N2 latency or N2-P2 amplitude were detected between the two subgroups of GBS patients with or without subjective lower limb paresthesia (P all >0.05). Moreover, there were no differences in N2 latency and N2-P2 amplitude among different groups when the waist was stimulated at the ASIS level. Our study suggested that CHEPs could be utilized as an objective and non-invasive tool to detect small myelinated fiber damage in GBS patients, especially for those without subjective paresthesia.

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